Atherosclerosis · 2021
Study on the association of wall shear stress and vessel structural stress with atherosclerosis: An experimental animal study.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Teng Zhongzhao, Wang Shuo, Tokgoz Aziz, Taviani Valentina, Bird Joseph, Sadat Umar, Huang Yuan, Patterson Andrew J, Figg Nichola, Graves Martin J, Gillard Jonathan H
Аннотация
BACKGROUND AND AIMS: Artery is subject to wall shear stress (WSS) and vessel structural stress (VSS) simultaneously. This study is designed to explore the role of VSS in development of atherosclerosis.
METHODS: Silastic collars were deployed on the carotid to create two constrictions on 13 rabbits for a distinct mechanical environment at the constriction. MRI was performed to visualize arteries' configuration. Animals with high fat (n = 9; Model-group) and normal diet (n = 4; Control-group) were sacrificed after 16 weeks. 3D fluid-structure interaction analysis was performed to quantify WSS and VSS simultaneously.
RESULTS: Twenty plaques were found in Model-group and 3 in Control-group. In Model-group, 8 plaques located proximally to the first constriction (Region-1, close to the heart) and 7 distally to the second (Region-2, close to the head) and 5 plaques were found on the contralateral side of 3 rabbits. Plaques at Region-1 tended to be bigger than those at Region-2 and the macrophage density at these locations was comparable. Minimum time-averaged WSS (TAWSS) in Region-1 was significantly higher than that in Region-2, and both maximum oscillatory shear index (OSI) and particle relative residence time (RRT) were significantly lower. Peak and mean VSS in Region-1 were significantly higher than those in Region-2. Correlation analyses indicated that low TAWSS, high OSI and RRT were only associated with plaque in Region-2, while lesions in Region-1 were only associated with high VSS. Moreover, only VSS was associated with wall thickness of plaque-free regions in both regions.
CONCLUSIONS: VSS might contribute to the initialization and development of atherosclerosis solely or in combination with WSS.
METHODS: Silastic collars were deployed on the carotid to create two constrictions on 13 rabbits for a distinct mechanical environment at the constriction. MRI was performed to visualize arteries' configuration. Animals with high fat (n = 9; Model-group) and normal diet (n = 4; Control-group) were sacrificed after 16 weeks. 3D fluid-structure interaction analysis was performed to quantify WSS and VSS simultaneously.
RESULTS: Twenty plaques were found in Model-group and 3 in Control-group. In Model-group, 8 plaques located proximally to the first constriction (Region-1, close to the heart) and 7 distally to the second (Region-2, close to the head) and 5 plaques were found on the contralateral side of 3 rabbits. Plaques at Region-1 tended to be bigger than those at Region-2 and the macrophage density at these locations was comparable. Minimum time-averaged WSS (TAWSS) in Region-1 was significantly higher than that in Region-2, and both maximum oscillatory shear index (OSI) and particle relative residence time (RRT) were significantly lower. Peak and mean VSS in Region-1 were significantly higher than those in Region-2. Correlation analyses indicated that low TAWSS, high OSI and RRT were only associated with plaque in Region-2, while lesions in Region-1 were only associated with high VSS. Moreover, only VSS was associated with wall thickness of plaque-free regions in both regions.
CONCLUSIONS: VSS might contribute to the initialization and development of atherosclerosis solely or in combination with WSS.